ArticleBritish journal of pharmacology2010
Trace amines depress D(2)-autoreceptor-mediated responses on midbrain dopaminergic cells.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Trace amine-associated receptor 1 (TAAR1): an emerging therapeutic target for neurodegenerative, neurodevelopmental, and neurotraumatic disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Pathophysiological Features of Nigral Dopaminergic Neurons in Animal Models of Parkinson's Disease.International journal of molecular sciences · 2022Review
- Trace amine-associated receptor 1 and drug abuse.Advances in pharmacology (San Diego, Calif.) · 2022Article
- Dopamine Evokes a Trace Amine Receptor-dependent Inward Current that is Regulated by AMP Kinase in Substantia Nigra Dopamine Neurons.Neuroscience · 2020Article
- AMP-activated protein kinase slows D2 dopamine autoreceptor desensitization in substantia nigra neurons.Neuropharmacology · 2019Article
- "TAARgeting Addiction"--The Alamo Bears Witness to Another Revolution: An Overview of the Plenary Symposium of the 2015 Behavior, Biology and Chemistry Conference.Drug and alcohol dependence · 2016Article
- Trace Amines and the Trace Amine-Associated Receptor 1: Pharmacology, Neurochemistry, and Clinical Implications.Frontiers in neuroscience · 2016Review
- Trace amine-associated receptor 1: A promising target for the treatment of psychostimulant addiction.European journal of pharmacology · 2015Review
- Activation of the trace amine-associated receptor 1 prevents relapse to cocaine seeking.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Article
- The role of β-adrenergic blockers in Parkinson's disease: possible genetic and cell-signaling mechanisms.American journal of Alzheimer's disease and other dementias · 2013Review
- Genetic deletion of trace amine 1 receptors reveals their role in auto-inhibiting the actions of ecstasy (MDMA).The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- The effects of pargyline and 2-phenylethylamine on D1-like dopamine receptor binding.Journal of neural transmission (Vienna, Austria : 1996) · 2011Article
- TAAR1 activation modulates monoaminergic neurotransmission, preventing hyperdopaminergic and hypoglutamatergic activity.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Electrophysiological effects of trace amines on mesencephalic dopaminergic neurons.Frontiers in systems neuroscience · 2011Article
- The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity.Journal of neurochemistry · 2011Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeAlthough trace amines (TAs) are historically considered 'false neurotransmitters' on the basis of their ability to induce catecholamine release, there is evidence that they directly affect neuronal activity via TA receptors, ligand-gated receptor channels and/or sigma receptors. Here, we have investigated the effects of two TAs, tyramine (TYR) and beta-phenylethylamine (beta-PEA), on electrophysiological responses of substantia nigra pars compacta (SNpc) dopaminergic cells to the D(2) receptor agonist, quinpirole. EXPERIMENTAL APPROACH: Electrophysiological recordings of D(2) receptor-activated G-protein-gated inward rectifier K(+) channel (GIRK) currents were performed on dopaminergic cells from midbrain slices of mice and on Xenopus oocytes expressing D(2) receptors and GIRK channels. KEY
resultsTYR and beta-PEA reversibly reduced D(2) receptor-activated GIRK currents in a concentration-dependent manner on SNpc neurones. The inhibitory effect of TAs was still present in transgenic mice with genetically deleted TA(1) receptors and they could not be reproduced by the selective TA(1) agonist, o-phenyl-3-iodotyramine (O-PIT). Pretreatment with antagonists of sigma1 and sigma2 receptors did not block TA-induced effects. In GTPgammaS-loaded neurones, the irreversibly-activated GIRK-current was still reversibly reduced by beta-PEA. Moreover, beta-PEA did not affect basal or dopamine-evoked GIRK-currents in Xenopus oocytes. CONCLUSIONS AND IMPLICATIONS: TAs reduced dopamine-induced responses on SNpc neurones by acting at sites different from TA(1), sigma-receptors, D(2) receptors or GIRK channels. Although their precise mechanism of action remains to be identified, TAs, by antagonizing the inhibitory effects of dopamine, may render dopaminergic neurones less sensitive to autoreceptor feedback inhibition and hence enhance their sensitivity to stimulation.
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